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Efficacy of induction therapy with ATG and intravenous immunoglobulins in patients with low-level donor-specific HLA-antibodies
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
 
ID 1192812
Author(s) Bächler, K; Amico, P; Hönger, G; Bielmann, D; Hopfer, H; Mihatsch, M J; Steiger, J; Schaub, S
Author(s) at UniBasel Mihatsch, Michael J.
Steiger, Jürg
Schaub, Stefan
Year 2010
Title Efficacy of induction therapy with ATG and intravenous immunoglobulins in patients with low-level donor-specific HLA-antibodies
Journal American journal of transplantation
Volume 10
Number 5
Pages / Article-Number 1254-62
Keywords Antibody-mediated rejection, ATG, HLA-antibodies, intravenous immunoglobulins
Abstract Low-level donor-specific HLA-antibodies (HLA-DSA) (i.e. detectable by single-antigen flow beads, but negative by complement-dependent cytotoxicity crossmatch) represent a risk factor for early allograft rejection. The short-term efficacy of an induction regimen consisting of polyclonal anti-T-lymphocyte globulin (ATG) and intravenous immunoglobulins (IvIg) in patients with low-level HLA-DSA is unknown. In this study, we compared 67 patients with low-level HLA-DSA not having received ATG/IvIg induction (historic control) with 37 patients, who received ATG/IvIg induction. The two groups were equal regarding retransplants, HLA-matches, number and class of HLA-DSA. The overall incidence of clinical/subclinical antibody-mediated rejection (AMR) was lower in the ATG/IvIg than in the historic control group (38% vs. 55%; p = 0.03). This was driven by a significantly lower rate of clinical AMR (11% vs. 46%; p = 0.0002). Clinical T-cell-mediated rejection (TCR) was significantly lower in the ATG/IvIg than in the historic control group (0% vs. 50%; p < 0.0001). Within the first year, allograft loss due to AMR occurred in 7.5% in the historic control and in 0% in the ATG/IvIg group. We conclude that in patients with low-level HLA-DSA, ATG/IvIg induction significantly reduces TCR and the severity of AMR, but the high rate of subclinical AMR suggests an insufficient control of the humoral immune response.
Publisher Munksgaard
ISSN/ISBN 1600-6135
edoc-URL http://edoc.unibas.ch/dok/A6003060
Full Text on edoc No
Digital Object Identifier DOI 10.1111/j.1600-6143.2010.03093.x
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/20353473
ISI-Number WOS:000276921600020
Document type (ISI) Journal Article
 
   

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